Wednesday, January 7, 2015

This article is written by Brooks Walsh, MD, an emergency physician, as well as Steve Smith, and with help from Ken Grauer, who is quite an ECG whiz. Brooks tackles the difficult issue of Persistent Juvenile T-waves (PJTWP). These are slightly asymmetrically inverted T-waves in V1-V3, but not beyond. The bottom line is that there is little firm guidance on the topic. SummaryPJTWP important considerations:1. Patients are typically African American women under age 30. It is rare in males over 19 years of age to have T-wave inversion beyond lead V1, unless there is lead misplacement or also possibly deep inspiration during recording (1).2. T-waves are slightly asymmetrically inverted in V1-V3. T-wave inversion that extends out to V4 and beyond should only be seen in patients under age 12.3. "Benign T-wave Inversion" is a different form of non-pathologic T-wave inversion. It does often extend out to V4 and beyond, has some ST elevation, and biphasic T-waves. It is seen primarily in young African American males.4. There are no structural cardiac abnormalities.5. The primary life-threatening pathologies on the differential diagnosis are a) Anterior ischemia (from pulmonary embolism or ACS) b) ARVD, Arrhythmogenic Right Ventricular Dysplasia (ARV Cardiomypathy). It is relatively rare, but causes deadly dysrhythmias.

ARVD: T-wave inversion in V1-V3, with the typical PJTWP morphology, but associated with

i) Syncope without a prodrome,

ii) PVCs with an LBBB morphology,

iii) Ventricular dysrhythmias, or iv) Epsilon waves of course are very specific but insensitive for ARVD

v) Males over age 19, definitely need further evaluation.

6. Although it is called "persistent", these T-waves may not always be persistent. Instead, like all benign findings, including early repolarization, it seems that they may be absent on a previous ECG and still be benign.Persistent juvenile T
wave pattern (PJTWP) – persistent confusion?

A
32-year African-American female came to the ED complaining of episodes of
palpitations and a “racing” heart. She had a history of DM and HTN. Vital signs
and the physical exam were unremarkable. An ECG was obtained:

Figure 1. There are assymetric T-wave inversions in V1-V3. Are these normal variants? Persistent Juvenile T-waves? Are these pathologic? Does she have "anterior" ischemia?

This
was compared with an ECG recorded 7 years prior:

Figure 2. This previous ECG also has TW inversions in V1 and V2 and a biphasic TW in V3. Does the ECG demonstrate a PJTWP?Does the fact that it was not fully present before preclude the diagnosis of PJTW?

This
is a difficult question to answer, but there have been a number of publications
in the last few years that shed some light on PJTWP. I’ll review 5 issues
that this literature highlights, then circle back to our patient.

Issue 1. Definition
of PJTWP

A
clear description of the PJTWP is surprisingly difficult to find.

Defining
true juvenile T wave patterns

It is worth revisiting the “true” juvenile T wave pattern. Recall that the RV of the
neonate has spent 9 months fighting the high-resistance pulmonary circulation,
and so the RV is (non-pathologically) hypertrophied. As a result, there may be ECG
findings of right ventricular dominance, including T-wave inversion (TWI) in leads V1-V3 or V4 in
young children. Generally, this pattern evolves to the adult pattern (i.e. TWI
limited to V1) by about 10 years of age.

Characteristics of “true” juvenile T wave pattern include shallow inversions, limited to V1-V3/V4,
an asymmetric morphology of the
inverted T wave, and no significant ST
segment deviation. For example, here is the ECG of a healthy 3 year-old
female:

Figure 3. We call these slightly asymmetric T-waves in V1-V3. Some would call these symmetric, in contrast to the very asymmetric T-waves of, for instance, Left Ventricular Hypertrophy below.

Figure 4. These are T-wave inversions that everyone would call asymmetric

For comparison, here are the symmetric T-waves of Wellens' Pattern B syndrome:

Figure 5. Note the near perfect symmetry of V2 and V3. This is NOT normal, not PJTWP.

An
example of a juvenile T wave pattern in a healthy 11 year-old male is provided
in an article by Sharieff and Rao:(3)

Figure 7. Here the T inversion is limited to V1 and V2; it is slightly asymmetric.

Defining
“persistent” juvenile T wave pattern in adults

There
are no consistent definitions of this adult variant of TWI. While one author
proposed “asymmetric T-wave inversions in
right precordial leads, without any other abnormalities”(4) as criteria, not all researchers agree.

For example, at least three articles
suggest that PJTWP is typically associated with significant ST segment
elevation in those same leads.(5, 6, 7)

Look at these closely, as we do not agree that this is PJTWP!

Uberoi

Figure 8. One complex of domed ST elevation preceding the TWI. This is not PJTWP, rather it is Benign T-wave Inversion (BTWI), also known as ST-T Normal Variant (STTNV) (8).

Choo 2002

Figure 9. Domed ST elevation preceding TWI -- we do not believe this is PJTWP, rather it is BTWI, the other normal variant

2009
Papadakis

Figure 10. Domed ST elevation preceding TWI -- we do not believe this is PJTWP, rather it is BTWI, the other normal variant

All
three of these ECGs show domed ST Elevation that precedes the TWI in the precordial
leads, a feature that is not usually
seen in children. This pattern has been termed “benign
T wave inversion” (BTWI) or “ST Elevation and Inverted T Wave” or ST-T Normal Variant (STTNV) by various authors. See numerous examples of BTWI here. In
contrast to PJTWP, this STE/TWI pattern of BTWI is found more often in males than
females,(8)and is considered by some to be a training-related variant. It is especially common in African American males.(

8)

Issue 2. PJWTP is
found more often in women.

Most
studies show that anterior TWI is found more often in women than men. In a
Finnish study, the distinct majority (87%) of the people with right-precordial
TWI were women (9), and a retrospective review done in
New Jersey also found a similar proportion.(4). On the other side of the world, in a
population of Israeli Bedouins, only women showed this pattern (10).

Issue 3. TWI (PJTWP or BTWI?) is
found more often in people of African heritage

Similar
to other atypical patterns of repolarization abnormalities, PJTWP appears to be
seen more common in patients of African heritage. In a cohort of black and
white females in the UK, 15% of the black females manifested TWI in anterior
leads, while only 4% of the white females did.(11). Similar results were seen in a cohort
of British and French athletes.(12). In a group professional American football
players, 4.3% of the black players showed this pattern, while only 1% of the
white players did.(6) A 2008 study found that TWIs (of
unspecified location) were far more common in black athletes than white.(13)Unfortunately, these studies are complicated by the confusion between PJTWP and BTWI patterns.

Issue 4. It may not be
part of the “athlete’s ECG.”

A
number of ECG variants have been described in highly trained athletes; e.g.
low-grade AV blocks, pseudo-LVH patterns, RSr', and early repolarization.(14) It is unclear, however, if anterior
TWI is part of this group of variants.

A
number of studies have suggested that anterior T wave inversions are more
common in athletes, and that they resolve with cessation of intense training.(15) However, Sharma found an equal
incidence of anterior TWI greater than 2 mm in
both athletes and non-athletes.(16)

Other
experts agree with this perspective.(17) Accordingly, at least 3 different
groups have recommended that athletes who have TWI in V2 and V3 should receive
further evaluation, even if currently asymptomatic.(5, 18, 19)

Issue 5. PJTWP is considered after ischemia, PE, and
ARVC have been excluded.

A
diagnosis of PJTWP should be arrived at only after consideration of more dangerous
causes of anterior TWI. Such ECG changes could reflect severe COPD,
PE, or pulmonary hypertension. Posterior MI or anterior ischemia should also be
ruled-out.

Arrhythmogenic
right ventricular cardiomyopathy (ARVC) is a rare disease, with ECG
manifestations that could be mistaken for PJTWP. Criteria for recognizing ARVC
on the standard ECG include “inverted T waves in right precordial leads (V1,
V2, and V3) or beyond in individuals greater than 14 years of age
(in the absence of complete right bundle-branch block QRS ≥120 ms)” as a major
criterion for diagnosis.”(20) Clearly, in the right context such as syncope, palpitations, or tachycardia, ARVC must be considered
before diagnosing PJTWP on the ECG.

The
2014 ECG shows asymmetric T wave inversion in leads V1 – V3, without ST segment
elevation or other concerning findings on the ECG. A review of her old ECGs
showed, however, that this TWI was not unchanged from prior, and was more
pronounced than 7 years ago. In particular, the T wave in V3 is now over 2 mm
deep.

A
cardiology consultation was obtained, serial troponin levels were negative, and
an echocardiogram from 3 years prior was found to be normal. She was discharged
from the ED with plans for outpatient follow-up with cardiology.

Figure 11. Note that the T-wave inversions in 2014 are deeper than in 2013. Can we prove that this is still normal? Or Abnormal?

Multiple ECGs were obtained in each patient, so that the chance of a technical error (lead placement) causing this pattern is unlikely. In case #1, 2 ECGs were obtained in different months of 2007 and 2014 and were consistent.
One may object that without definitive evaluation using echocardiography, angiography, MRI, etc., that we cannot be certain that the TWI is not due to an undiagnosed structural disorder, including ARVD. Evaluation was pursued only to the degree that the indivudual clinician felt was warranted for the presenting complaint.
On the other hand, we are not aware of any longitudinal studies of normal populations which confirm that what appears to be PJTWP does NOT develop later. We do know that many T-wave inversion patterns are benign.
Given that this pattern is commonly presumed to be benign, clinicians may have "underinvestigated" the ECG findings in this case. Biases about TWI in female African American patients may play a role in limited investigation, leading to premature diagnostic closure.
These limitations argue for reconsidering the benignity of PJTWP.
So
– can you diagnose PJTWP if the pattern is not,
in fact, persistent? Despite the number of new articles on the subject, there
is no guidance here.

Furthermore,
as discussed in Issue #1 above, much of the literature regarding PJTWP includes
ECGs with significant ST elevation in the anterior leads, a distinctly unjuvenile pattern. How distinct is
this STE/TWI pattern from “true” PJTWP? Is it a minor variant, or is it
clinically important? Again, the answer isn’t clear from the recent results.

I
guess you could say that our case and review suggest that “persistent juvenile”
T wave pattern may be neither persistent nor juvenile.

12 comments:

Well done discussion by Brooks Walsh (!) - who confronts key issues on distinction between PJTWP vs other potentially more serious conditions. I'll expand on a few points:

"Symmetry" of T waves is in the eyes of the beholder. Whether one calls a T wave "symmetric" or "asymmetric" depends in large part on what one calls the onset of the "T" wave (vs the end of the ST segment). Best illustration of this concept lies with the 1st and 3rd QRS complexes in lead V6 of Figure 4 - in which the ST segment sags (slow downslope) on its way to a T wave that then quickly returns to the baseline. There is baseline wander in V5 of Figure 4 - but if one uses a late onset for the beginning of the T wave for the middle complex in lead V5 of Fig. 4 - there really is not the typical asymmetry of LV "strain" ... That said - there can be NO DOUBT that the deep T wave inversions in V2,V3,V4 of Figure 5 are clearly symmetric by any definition that one might use. The relevance of this admittedly "picky" point is for each of us to develop our own consistent internal definition for how the T wave inversion in lead V3 of Figure 6 (due to PJTWP) looks different from the ischemic-looking inverted T waves in leads V2,V3,V4 of Figure 5.

Near the end of Brooks' discussion - he raises the question of whether discharge of this patient from the ED was justified without more "definitive evaluation" including Echo, angiography, MRI, etc. The dilemma of how far to go with one's workup in ruling out all possible pathology is never-ending - especially in emergency medicine. One just doesn't want to miss that "needle in the haystack that might lead to the patient's demise". But in this case - looking for entities such as ARVD is truly looking for a needle in a haystack. ARVD is rare - and the number of false positives one is destined to uncover if full evaluation is done for all patients with anterior T wave inversion is innumerable. Often overlooked is the potential for harm by doing extra work-ups (which will doubtlessly uncover incidentalomas leading to more downstream testing with usually negligible real yield). Additional work-up for the 2014 ECG in this case is simply not needed.

Finally - I think it important to realize the subtleties of comparing sequential tracings for differences. I completely agree with Brooks that it DOES look like the anterior T wave inversion in this case has increased - but arriving at this conclusion is not as simple as might appear. Note in Figure 11 the difference in QRS amplitude between the 2 tracings - with early transition (between V2-to-V3) in 2007 - whereas the QRS remains isoelectric in V3 in 2014. Lead V2 in 2014 might be misplaced - as its QRS amplitude is inexplicably greater than V3. And returning to Figures 1 and 2 (showing the full 12-leads for 2007 vs 2014) - the frontal plane axis is not the same in the 2 tracings, and the T wave in lead III is negative in 2014 (whereas it wasn't inverted in 2007 ( = S1Q3T3 pattern in 2014). And supporting my theory that there was some lead misplacement in 2014 are the much more abrupt morphology changes compared to the more consistent development of R wave amplitude in V3-thru-V6 seen in Figure 2.

If I wrote that, then I was mistaken. Can you show me the case where I did so? What I would have meant to write is this: "if the choice is between ACS and PE because of T-wave inversion in V1-V3, then T-wave inversion in III makes it much more likely to be PE." This is from 2 studies by Kosuge et al. Here is one:

Thank you for this great post.I have a couple of questions:1.If the pacient with the Figure 1. EKG had chest pain, wouldn't PE be on top of the differential diagnosis?(at a glance this EKG http://hqmeded-ecg.blogspot.com.au/search/label/pulmonary%20embolism?updated-max=2013-12-20T12:08:00-06:00&max-results=20&start=3&by-date=false looks similar- even if for an expert there are differences)

2.Would a pacient with figure 10. EKG and recently resolved chest pain be suspected of Wellens syndrome- pattern A ? (http://hqmeded-ecg.blogspot.com.au/search/label/Wellens%27%20syndrome) - more to the point how could we be sure if Benign T-wave Inversion is realy benign without coronarography?

Adi,Thanks for the great questions.There are subtle differences.Question 1: the PE you reference has T-wave inversion all the way out to V6, which should never be assumed to be benign. All the cases I have posted of PE here have either T-wave inversion beyond V3, or some ST elevation: http://hqmeded-ecg.blogspot.com/search/label/pulmonary%20embolism?updated-max=2013-12-20T12:08:00-06:00&max-results=20&start=3&by-date=false

Question 2: Notice that in figure 10 there is a very tall R-wave AND a J-wave in V4 and V5. These are typical of BTWI and NOT of Wellens'.

Thank you for clearing that up for me.Maybe you should consider talking in a post about the different causes of T wave inversion in the precordial leads( for example PE sometimes looks like Wellens' Syndrome for someone which is less experienced ) and how to differentiate between them.Thank you again for this great learning experience.

I have found that comparing the onset of the inverted T wave to the point at which it returns to the baseline is very helpful in determining symmetry vs. asymmetry. If the angles formed by the departure from, and the return to, the baseline are basically the same, then the inverted T is symmetrical. If the angle at the beginning of the inverted T is different than at the end of the T (usually obtuse vs. acute), then it's asymmetrical.

Thanks for this comprehensive review.I can see TWI in leads II and aVF and flat T wave in the first ecg presented that weren't exist 7years ago..Is this significant ? ..And are these tiny q waves in the same 3 leads significant?

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